The introduction of new platelet glycoprotein (GP) IIb/IIIa receptor inhibitors has the potential to revolutionize the treatment of certain patients with unstable angina and non-ST-segment elevation myocardial infarction (MI). Treatment with these potent platelet inhibitors has been shown to improve patient outcomes prior to percutaneous intervention (PCI), following PCI, and even in the absence of PCI. In addition, there are data from clinical studies that support a time-dependence to the beneficial effects of platelet inhibitor therapy. Patients who are treated early-for example, in the emergency department (ED)-appear to have improved outcomes over those treated later. Platelet inhibitors have been used extensively in the cardiac catheterization laboratory and in the coronary care unit (CCU). In many institutions, however, their introduction and uptake in the ED has been slow. These agents are relatively expensive and have the potential to cause major bleeding complications. This review will examine the pathophysiology of acute coronary syndromes (ACS) as it relates to the mechanism of action of GPIIb/IIIa inhibitors. The available GPIIb/IIIa inhibitors will be discussed including their indications, contraindications, doses, and mechanisms of action. Data from clinical studies supporting the use of GPIIb/IIIa inhibitors will be illustrated in the context of their applications in the ED. Finally, an algorithm for GPIIb/IIIa inhibitors in the ED will be presented.